Table. 3 A summary of published studies on enhancer-based subtypes of cancer.
From: Enhancer reprogramming: critical roles in cancer and promising therapeutic strategies
Cancer type | Size of sample | Features for subtyping | Identified/Characterized subtypes | Multi-omics characterization | References |
|---|---|---|---|---|---|
Acute myeloid leukemia | 66 patients and 28 cell lines | SE H3K27ac signal | Six novel subtypes: C1, C2, C3, C4, C5, C6. | H3K27ac ChIP-seq; somatic mutation; RNA-seq, | [411] |
Gastric cancer | 23 patients and 26 cell lines | SE H3K27ac signal | Two subtypes: Mes and nMes | H3K27ac and H3K4me1 ChIP-seq; ATAC-seq | [412] |
Gastric cancer (Peritoneal metastasis) | 98 patients and 59 cell lines | SE H3K27ac signal | Two subtypes: EMT group (characterized by SMAD3 as the only master TF, followed by RUNX1, BHLHE40 and TEAD1) and non-EMT group (enriched in ELF3 and KLF5) | H3K27ac ChIP-seq; DNA methylation analyses; RNA-seq; WGS analyses; CNV | [413] |
Pancreatic cancer | 24 human PDAC samples grown as patient-derived tumor xenografts (PDTXs) | SE H3K27ac signal | Two subtypes: the classical subtype and the basal subtype | H3K4me1, H3K27ac, H3K4me3 H3K27me3 and H3K9me3 ChIP-seq; whole-genome DNA methylation analysis; RNA-seq; SNP arrays analysis | [414] |
Lung cancer (lung adenocarcinoma,LUAD) | 42 patients | SE H3K27ac signal | Two groups: GI represents the more aggressive tumor while GII represents the less aggressive one. | H3K27ac ChIP-seq, RNA-seq | [415] |
Lung cancer (lung squamous cell carcinoma, LUSC) | 13 cell lines | SE H3K27ac signal | Two subtypes: the novel “neural” subtype, defined by SOX2 and Brn2, and “classical” subtype, defined by SOX2 and p63. | H3K27ac ChIP-seq; RNA-seq | [416] |
Lung cancer (small-cell lung cancer, SCLC) | 25 cell lines | SE H3K27ac signal | Four known clusters: SCLC-A, SCLC-N, SCLC-P, SCLC-Y, and two novel subtypes among SCLC-A: SCLC-Aα and SCLC-Aσ. | H3K27ac ChIP-seq; RNA-seq | [386] |
Neuroblastoma | 60 patients and 25 cell lines | SE H3K27ac signal | MYCN-amplified, MYCN non-amplified high-risk, MYCN non-amplified low-risk; A novel subtype, exhibiting mesenchymal characteristics, shared cellular identity with multipotent Schwann cell precursors, and RAS activated. | H3K27ac and H3K4me3 ChIP-seq; HiCHiP; ATAC-seq; RNA-seq | [417] |
Prostate cancer | 100 patients | SE H3K27ac signal | Three clusters: Cl1, Cl2 and Cl3 | AR, H3K27ac, H3K4me3, and H3K27me3 ChIP-seq; RNA-seq | [418] |
Glioblastoma | 50 fresh-frozen tumor specimens, 20 patient-derived GPCs, and 5 established GBM cell lines | SE H3K27ac signal | Four subtypes: AC1-mesenchymal, AC1-classical, AC2-proneural, and AC3-proneural | H3K27ac ChIP-seq; RNA-seq; Sanger sequencing | [419] |
Medulloblastoma | 28 patients and 3 cell lines | SE H3K27ac signal | Four subtypes: WNT, SHH, Group 3, and Group 4. | H3K27ac, BRD4, H3K27me3, H3K4me1, LMX1A, LHX2, and HLX ChIP-seq; RNA-seq; 4C-seq; DNA methylation, CNV | [390] |
Breast cancer | 19 cell lines | SE H3K27ac signal | Two groups: TNBC and non-TNBC | H3K27ac, H3K4me1, H3K4me3, H3K27me3 ChIP-seq | [420] |
Colorectal cancer | 69 samples and 11 cell lines | SE H3K27ac signal | Four subtyps: EPiC1,EPiC2,EPiC3 and EPiC4. | H3K4me1, H3K4me3,H3K79me2,H3K9me3 and H3K27me3 ChIP-seq | [421] |
Renal cell carcinoma | 42 patients | SE H3K27ac signal | Three subtypes: ccRCC, pRCC, chRCC | H3K27ac and H3K4me2 ChIP-seq; ATAC-seq; RNA-seq; SNP arrays analysis | [422] |
Bladder cancer | 4 patients and 4 cell lines | SE H3K27ac signal | Two subtypes: luminal and basal. | H3K27ac ChIP-seq; RNA-seq; ATAC-seq; Hi-C | [423] |
15 patients and 9 cell lines | SE H3K27ac signal | Two subtypes: luminal and basal. | H3K27ac, H3K27me3 and H3K9me3 ChIP-seq; RNA-seq | [410] | |
Multiple myeloma | 30 patients and 5 cell lines | Chromatin accessibility and paired transcriptome profiles | Four subtypes: MAF, CCND1, HD, and MMSET. | H3K27ac ChIP-seq, ATAC-seq; RNA-seq | [424] |
